Figure 1
T2WI Coronal
Bilateral hippocampal atrophy with dilatation of temporal horns.
Neuro-degenerative diseases
SectionNeuroradiology
Case TypeClinical Cases
Authors
Mazhar Shaikh M, Nadkarni DS.
Radiance Diagnostics, MRI Unit.
Connected authors
70 years, male
Clinical History
A 70-year-old male patient presented with a history of progressive forgetfulness for the past few months. H/o involuntary movements of the head and upper extremities was noted.
No h/o weakness. No h/o past vascular insult/stroke. On examination no focal neurological deficit seen.
No h/o weakness. No h/o past vascular insult/stroke. On examination no focal neurological deficit seen.
Imaging Findings
• Severe grey matter atrophy involving both the cerebral hemispheres, with more predominant volume loss in both temporal lobes. Atrophy of hippocampal formations also noted.
• The subarachnoid spaces were prominent with dilated ventricular system particularly the temporal horns. The sylvian fissures appeared markedly widened.
• The brainstem appeared normal. Pars compacta showed normal thickness on both sides.
• No focal white matter abnormality detected.
• MR Spectroscopy revealed increase in Myo-inositol and reduced levels of NAA
• The subarachnoid spaces were prominent with dilated ventricular system particularly the temporal horns. The sylvian fissures appeared markedly widened.
• The brainstem appeared normal. Pars compacta showed normal thickness on both sides.
• No focal white matter abnormality detected.
• MR Spectroscopy revealed increase in Myo-inositol and reduced levels of NAA
Discussion
Alzheimer’s disease is the most common acquired brain degenerative disease and also most common form of dementia, which constitutes 60 to 70 % of all cases.
Pathologically Alzheimer’s is characterised by damage to the large cortical neurons subserving cognition, initially in the temporal lobes and later in the remaining neo cortex and association areas. Damage is believed to occur owing to mechanism outside as well as inside the neuron and is characterised by the appearance of extracellular senile (amyloid) plaques and intracellular neurofibrillary tangles.
Alzheimer’s is a progressive degenerative disorder of insidious onset, characterised by memory loss, confusion and a variety of cognitive disabilities.
It may occur as early as the age of 40 years, but is most commonly seen after the age of 60 years. The cause is unknown; however, it seems to have a familial incidence indicating a strong genetic component. The diagnosis of this disease can be made with high accuracy by using clinical, neuropsychological and imaging assessments.
MRI scores over CT for the routine evaluation of Alzheimer’s. Coronal MR images are useful to document or quantify atrophy of the hippocampus and medial temporal lobes.
On MRI Alzheimer’s patients show generalised cortical atrophy and grey matter reduction with disproportionate volume loss in the anterior temporal lobes and hippocampi (hallmark features). The temporal horns as well as the choroid and hippocampal fissures appear particularly prominent. Enlarged sylvian fissure are sensitive.
In Alzheimer’s the presence of senile plaques is associated with neuronal loss that is reflected as decrease in the N-Acetyl Aspartate. Additional finding is increase in the Myo-Inositol which is a metabolite of astrocytes, surrounding the senile plaques.
Cholinesterase inhibitors are a major therapy for treating memory loss symptoms by prolonging the presence of acetylcholine at remaining cholinergic synapses, thereby aiding in signal transmission. Although memory initially improves, it subsequently deteriorates because senile plaques and neurofibrillary tangles continue to develop and destroy neurons.
Over time, patients with AD can display anxiety, depression, insomnia, agitation, and may become violent and paranoid and even lose all bodily function, including the ability to walk and swallow. The time from diagnosis to death varies from as little as 3 years if the patient is older than 80 years when diagnosed to as long as 10 or more years if the patient is younger. The primary cause of death is intercurrent illness, such as pneumonia.
Pathologically Alzheimer’s is characterised by damage to the large cortical neurons subserving cognition, initially in the temporal lobes and later in the remaining neo cortex and association areas. Damage is believed to occur owing to mechanism outside as well as inside the neuron and is characterised by the appearance of extracellular senile (amyloid) plaques and intracellular neurofibrillary tangles.
Alzheimer’s is a progressive degenerative disorder of insidious onset, characterised by memory loss, confusion and a variety of cognitive disabilities.
It may occur as early as the age of 40 years, but is most commonly seen after the age of 60 years. The cause is unknown; however, it seems to have a familial incidence indicating a strong genetic component. The diagnosis of this disease can be made with high accuracy by using clinical, neuropsychological and imaging assessments.
MRI scores over CT for the routine evaluation of Alzheimer’s. Coronal MR images are useful to document or quantify atrophy of the hippocampus and medial temporal lobes.
On MRI Alzheimer’s patients show generalised cortical atrophy and grey matter reduction with disproportionate volume loss in the anterior temporal lobes and hippocampi (hallmark features). The temporal horns as well as the choroid and hippocampal fissures appear particularly prominent. Enlarged sylvian fissure are sensitive.
In Alzheimer’s the presence of senile plaques is associated with neuronal loss that is reflected as decrease in the N-Acetyl Aspartate. Additional finding is increase in the Myo-Inositol which is a metabolite of astrocytes, surrounding the senile plaques.
Cholinesterase inhibitors are a major therapy for treating memory loss symptoms by prolonging the presence of acetylcholine at remaining cholinergic synapses, thereby aiding in signal transmission. Although memory initially improves, it subsequently deteriorates because senile plaques and neurofibrillary tangles continue to develop and destroy neurons.
Over time, patients with AD can display anxiety, depression, insomnia, agitation, and may become violent and paranoid and even lose all bodily function, including the ability to walk and swallow. The time from diagnosis to death varies from as little as 3 years if the patient is older than 80 years when diagnosed to as long as 10 or more years if the patient is younger. The primary cause of death is intercurrent illness, such as pneumonia.
Differential Diagnosis List
Alzheimer's disease
Age-related brain atrophy
Lewy-body disease
Pick\'s dementia
Vascular dementia
Parkinsonism/Parkinsonism-related disease
Final Diagnosis
Alzheimer's disease
Case information
| URL: | https://www.eurorad.org/case/9324 |
| DOI: | 10.1594/EURORAD/CASE.9324 |
| ISSN: | 1563-4086 |
Figure 2
T2WI Axial
Grey matter atrophy, predominantly in the temporal lobes with dilated sylvian fissures.
Figure 3
T2WI Corornal
Severe volume loss of temporal lobes.
Figure 4
MR Spectroscopy
MR Spectroscopy reveals increase in myo-inositol and decreased NAA levels.
T2WI Coronal
Bilateral hippocampal atrophy with dilatation of temporal horns.
T2WI Axial
Grey matter atrophy, predominantly in the temporal lobes with dilated sylvian fissures.
T2WI Corornal
Severe volume loss of temporal lobes.
MR Spectroscopy
MR Spectroscopy reveals increase in myo-inositol and decreased NAA levels.